Cells of the immune system are recruited from the bloodstream to areas of tissue inflammation, damage or infection, resulting in an accumulation of immune cells at the affected site. A marked infiltration of immune cells often occurs in injured or diseased organs. For example, myocardial infarction (MI) is such an injury. In this process, myocardial tissue comprising a portion of the left ventricle
(LV) is injured because it is denied oxygen acutely. This insult sets off a sequence of inflammatory events that culminates in replacement of functional myocardial tissue with non-functional scar tissue. The diminished pumping efficiency in the scarred LV places stress on the remaining viable LV myocardium, which becomes dysfunctional over time, eventually forming more scar tissue. This “scar begetting” phenomenon underlies the clinical sequelae of MI, including heart failure and arrhythmias, which engender mortality, morbidity, and high cost.
With the goal of minimizing scar burden, the optimum time to intervene after MI is early, before the default pathways have had time to replace dead LV myocardium with scar. Over the past several years, there has been increasing interest in manipulating these pathways so as to convince the body to replace dead myocardium with new, functional myocardium. This interest centers on the introduction of biological materials, including certain cells (e.g., stem and/or precursor cells) and/or proteins that possess such manipulative capabilities.
MI is just one example in which internal organs are injured; resulting in inflammation and possible scarring. More generally, there remains a need for accurate delivery of medicaments to injured internal organs, as well as precise diagnosis of abnormalities and lesions associated with internal organs.